1. Field of the Invention
The present invention relates to ventilation of patients during anesthesia, and more particularly relates to a method and apparatus for maintaining and monitoring alveolar ventilation, carbon dioxide excretion and oxygenation in patients who receive general anesthesia.
2. Background Information
General anesthesia induces a state of respiratory insufficiency. Most general anesthetic agents cause a decrease in central drive for respiration, which unimpeded may cause a decrease in oxygenation and increase in arterial blood carbon dioxide tension (PaCO.sub.2). In addition, general anesthetic agents decrease respiratory muscle strength. This especially is true of paralytic agents, such as curare, which may remove any ability of the patient to breathe. In addition, general anesthesia has been shown to decrease compliance of the lung and thoracic cage. A decrease in the compliance of these structures requires an increase in muscle strength to produce adequate ventilation, in the absence of mechanical ventilatory assistance.
Anesthetic agents are known to have several effects, which may impede the efficiency of oxygenation. General anesthesia is associated with a decrease in the functional residual capacity (FRC) of the lung, the volume of gas remaining within the lung at the end of normal exhalation. Decrease in FRC will cause a regional decrease in ventilation (V.sub.A) relative to perfusion (Q), which may cause decrease in arterial blood oxygenation (PaO.sub.2). It has been shown that hypoxic pulmonary vasoconstriction (HPVC) is rendered less active by several anesthetic agents. Release of HPVC will cause an increase in perfusion to poorly ventilated lung units, causing PaO.sub.2 to decrease. In addition, it has been shown that the current methodology for delivering positive pressure ventilation will cause flow of gas to be directed to dependent lung regions to a greater extent than to non-dependent lung regions. Yet, gravity directs the flow of blood to more non-dependent lung regions. Therefore, less ventilation and more perfusion will be directed to dependent areas of the lung, causing decrease in V.sub.A /Q and relative arterial hypoxemia (decreased PaO.sub.2).
General anesthesia is likely to result in inadequate alveolar ventilation and hypercarbia (increase PaCO.sub.2) and inadequate arterial oxygenation (arterial hypoxemia), unless active intervention is applied. For these reasons, positive pressure ventilation is commonly applied to mechanically augment pulmonary ventilation during general anesthesia. In addition, an increase in inspired oxygen concentration is almost always employed, to overcome the arterial hypoxemia producing effects of general anesthesia. Occasionally, a positive end-expiratory pressure (PEEP) is applied to the mechanical ventilatory pattern, in order to increase FRC and improve arterial oxygenation.
Conventional positive pressure ventilation produced with a mechanical ventilator is associated with several undesirable side-effects. Positive pressure ventilation causes physical movement of the lung, chest wall and diaphragm. As a result, any surgical field except for the head, neck and extremities will be subject to undesired movement for a considerable portion of the respiratory cycle. Only during the period of time from end-expiration to initiation of positive pressure breath will the surgical field be still. As mentioned above, both extremes of V.sub.A /Q abnormality will be created by positive pressure ventilation, as created by a standard anesthesia ventilator. An increase in V.sub.A /Q causes increase in alveolar dead space, lung which is ventilated, but not perfused. Decrease in V.sub.A /Q will cause decline in efficiency of oxygenation of the arterial blood. An increase in airway pressure created by positive pressure ventilation will increase intrapleural pressure, decrease venous return and decrease cardiac output. During standard positive pressure ventilation with an anesthesia ventilator, no spontaneous respiratory activity may occur, due to lack of sufficient flow of respiratory gases from the anesthesia circuit. Furthermore, standard positive pressure ventilation from an anesthesia ventilator often results in excessive removal of CO.sub.2, increase in arterial blood pH and the well known adverse effects of respiratory alkalosis.
During general anesthesia, monitoring of respiratory function is critically important. Subtle changes in the mechanics of respiration indicate to the anesthesiologist important information with respect to the cardiorespiratory system, such as bronchoconstriction, pulmonary edema and airway obstruction. Changes in pulmonary gas exchange must be monitored for accurate determination of adequacy of alveolar ventilation and oxygenation. Unfortunately, standard mode positive pressure ventilation during general anesthesia with existing equipment makes such monitoring relatively inaccurate and difficult.
Most anesthesia ventilators deliver inspirable gas at a flow rate such that airway pressure is increased excessively, secondary to resistance of the tracheal tube and the patients' large airways. Thus, assessment of small airways resistance is extremely difficult. Institution of an inspiratory hold often is applied to assess airways resistance. However, application of such an inspiratory hold will result in a marked increase in mean airway pressure and intrapleural pressure and decrease in venous return and cardiac output. In addition, such an inspiratory hold significantly decreases the time of stability of the surgical field.
Conventionally, it has been held that the end-tidal carbon dioxide tension (P.sub.ET CO.sub.2) is an index of alveolar ventilation. Ideally, P.sub.ET CO.sub.2 is equivalent to PaCO.sub.2, but this is true only if all alveoli are perfused and alveolar dead space is nonexistent. However, studies have repeatedly shown that positive pressure ventilation applied with a standard anesthesia ventilator tends to cause an increase in alveolar dead space and inaccuracy of monitoring of alveolar ventilation. Therefore, in order to asses adequacy of ventilation during general anesthesia, analysis of arterial blood to measure PaCO.sub.2 is necessary.
During the expiratory phase of the respiratory cycle, currently existing means of mechanical ventilation do not allow an active flow of gas from the reservoir bellows. Any flow of gas from the bellows results in a decrease in airway pressure, during the expiratory phase of the respiratory cycle. Thus, any inspiratory effort by the patient during the expiratory phase of the ventilator cycle will result in a decrease in airway pressure. This decrease in airway pressure will cause undesirable decrease in intrapleural pressure, which may cause significant deterioration of cardiovascular function, secondary to afterload of the left ventricle of the heart and will increase work of breathing. For this reason, spontaneous ventilation is not allowed when a mechanical ventilator is employed during general anesthesia. Spontaneous ventilation is permitted only when a standard anesthesia circuit employing a non-encased anesthesia reservoir bag is employed. In addition, anesthesia circuitry does not permit the application of a continuous positive airway pressure (CPAP) during spontaneous respiration. Thus, the only way to maintain a positive airway pressure during the expiratory phase of the respiratory cycle, positive end-expiratory pressure (PEEP), is to maintain complete control of the patients' respiratory function. This causes marked increase in mean airway pressure, mean intrapleural pressure, and significant decrease in venous return and cardiac output. In addition, it has been shown that an increase in mean airway pressure during controlled mechanical ventilation will significantly increase ventilation (V.sub.A) relative to perfusion (Q) in many areas of the lung. Such an increase in V.sub.A /Q will increase physiologic dead space, with its attendant undesirable effects.
As detailed above, it is well known and accepted medical practice that patients receiving general anesthesia require mechanical ventilatory support. In almost all cases, this is accomplished using a semi-closed system with a CO.sub.2 absorbent that will allow partial rebreathing of anesthetic gases. Some systems employ sufficiently high gas flow to prevent significant rebreathing of anesthetic gases, so that CO.sub.2 absorption is unnecessary. Nearly complete rebreathing of anesthetic gases is rarely accomplished without CO.sub.2 absorption, but when attempted control of arterial CO.sub.2 tension is maintained with a fresh gas flow into the rebreathing circuit in an amount necessary to maintain arterial blood CO.sub.2 tension at an acceptable level and a total ventilation of at least 3 times the level of fresh gas inflow. With these systems, a collapsible reservoir of variable capacity is alternately compressed and allowed to relax by application and release of positive pressure from a compressed gas source. Usually, this reservoir consists of a concertina bag, housed within a rigid, clear container. The concertina bag is typically filled from below, so that inspiration to the patient consists of a fall in the bellows secondary to externally applied pressure within the rigid container. Exhalation from the patient results in gas entering the bellows, causing it to rise within the container. The volume of gas delivered by the positive pressure breath is determined by the height of the bellows within the cylinder prior to inspiration and the distance that the bellows travels during the inspiratory phase of the ventilatory cycle. Various means of controlling volume delivery and inspiratory pressure have been devised. These include regulation of flow into the rigid chamber, time allowed for inspiration, and mechanical limitation of the excursion of the bellows.
Various types of ventilators have been developed for patients afflicted with acute lung injury and/or respiratory failure. Among the conventional mechanical ventilation techniques are assist mechanisms, intermittent mandatory ventilation (IMV), positive end-expiratory pressure (PEEP) and high frequency low-tidal volume therapy, such as applied in infant ventilation. U.S. Pat. No. 4,773,411 to Downs, the disclosure of which is incorporated herein by reference, discloses an apparatus for applying continuous positive airway pressure to patients with respiratory disorders. The disclosed apparatus achieves augmentation of alveolar ventilation and carbon dioxide excretion through intermittent cycles of reduced airway pressure below the CPAP pressure level. The apparatus is used to provide ventilatory assistance to patients with impaired spontaneous respiration capability.
Despite the above-noted developments, a need exists for an apparatus and associated method that can, in combination, maintain alveolar ventilation, carbon dioxide excretion and oxygenation in patients during general anesthesia.